Electrophysiological techniques were used to characterize the ionic channels of neurons isolated from slices of the adult guinea pig thalamus. Thalamic neurons undergo a shift from tonic to phasic (burst) firing upon hyperpolarization. This state transition results from deinactivation of a regenerative depolarizing event referred to as the low-threshold spike (LTS). Isolated thalamic (dorsal lateral geniculate) neurons exhibited low-threshold spikes that could be blocked by low concentrations of nickel, but were unaffected by the dihydropyridine nimodipine. Whole cell voltage clamp recordings from these cells demonstrated a low-threshold, rapidly inactivating (T) calcium current that manifested similar voltage-dependency and time course as the low threshold spike. Like low threshold spikes, the T type calcium current was eliminated by nickel but was unaffected by nimodipine. In thalamic neurons, T type calcium channels underlie the low threshold spike, and therefore play a critical role in regulating the firing pattern of these cells. Hodgkin-Huxley modeling of the LTS indicated that its shape can be accounted for almost entirely by the intrinsic properties of T-type voltage-dependent calcium channels. Burst firing mediated by the LTS is critical to the generation of absence seizures and drugs which specifically block the LTS (T-type calcium channels) prevent absence seizures. Therefore, isolated thalamic neurons are likely to be a useful experimental system for the evaluation of potential new antiabsence drugs.